1. Field of the Invention
This invention is a system and method for stimulating a heart of a patient. More specifically, it is a stimulation device assembly and method using a stimulator coupled with an implantable emitter that is in turn coupled with a conductive agent injected into the region of the heart to be stimulated.
2. Description of the Background Art
Various medical device systems and methods have been disclosed for coupling energy to cardiac tissue in order to influence heart function. A great many of such systems and methods have been disclosed for the particular purpose of treating various types of cardiac arrhythmias, including for example fibrillation, tachycardia, bradycardia, or other arrhythmias.
Among the many different devices and methods previously disclosed for energy coupling to cardiac tissue, various different types of energy coupling have also been employed.
One type of energy coupling having significant impact over the years in treating cardiac arrhythmias delivers energy into targeted regions of cardiac tissue using energy emitters in or around the heart. Various previously disclosed examples of energy delivery systems and methods of this type include devices using: emitters of electrical energy, e.g. electrodes for delivering direct or alternating current, such as radiofrequency (RF) current; emitters such as crystals or transducers for delivering sonic energy (e.g. ultrasound); emitters such as fiber optics, lenses, or other light discharge elements (e.g. laser diodes) for delivering light (e.g. laser); or energy emitters using microwave coupling (e.g. induction).
Another type of energy coupling that has been investigated for treating certain cardiac arrhythmias includes hypothermia or cryogenic devices intended to reduce tissue temperature to a level. In general, these devices include regions that are cooled to low temperatures (relative to surrounding body temperature) so as to thereby pull heat from and reduce the temperature in surrounding tissue. By achieving this heat transfer at sufficient levels, an intended change in the affected tissue structure or function, either temporarily or permanently. To the extent that such hypothermic coupling relates to pulling thermal energy from the surrounding tissue so as to cool it, such devices are considered energy coupling devices.
The designs and features of the various different energy coupling devices for cardiac treatment also vary in order to adapt such devices to achieve different intended results.
For example, certain such devices and methods generally herein referred to as “ablation devices” are specifically adapted to couple sufficient energy with cardiac tissue so as to ablate the tissue. This may be performed for example in order to terminate a focal origin of arrhythmia, or to form a conduction block to terminate a harmful conduction pathway within the cardiac tissue network causing arrhythmia.
Other ablation devices have also been disclosed for the purpose of forming passageways through tissue or other material located within a patient, such as for recanalization of occluded lumens and vessels.
Other previously disclosed examples of cardiac treatment devices using energy coupling have been specifically adapted to stimulate cardiac tissue, rather than to ablate it. Various types of these cardiac stimulation systems include: devices adapted to couple energy to cardiac tissue in a manner so as to trigger an arrhythmia in order to diagnose cardiac conduction through the heart; pacemaker assemblies and methods adapted to provide artificial pacing of the cardiac cycle in order to cure an arrhythmia; and defibrillator assemblies and methods wherein the heart is “shocked” out of an arrhythmia and back into sinus rhythm.
Because the cardiac conduction cycle is directly and intimately related to electrical conduction through cardiac tissue, the previously disclosed cardiac stimulation devices for triggering, pacing, or defibrillating, are generally electrical coupling devices that deliver electrical energy from electrode leads or catheters secured to or placed against the tissue to be stimulated. Pacemaker and defibrillator assemblies have each been adapted with varied (and in some regards mutually exclusive) designs appropriate to suit one or the other of temporary or permanent use, depending upon a particular need for either acute or chronic rhythm management, respectively.
In general, permanent pacemaker systems include a pacemaker assembly with a pacemaker coupled to an electrical lead generally called a “pacemaker lead”. The implantable or permanent pacemaker typically includes a power source, such as a source of electrical current energy (e.g. a battery). This power source is electrically coupled to one end of the electrical lead. The other end of the electrical lead is in turn coupled to the cardiac tissue to be stimulated, usually by use of an anchor such as a needle, screw, spline, grasper, etc., which anchor may be the electrode current emitter itself.
In recent years, an increasing amount of interest, and research and development, has been directed toward modifying the cellular make-up of cardiac tissue structures in order to enhance cardiac conduction or function in such modified structures.
Certain such efforts have been directed toward delivering conductive, contractile muscle cells into regions of the heart where contraction is compromised, such as areas of necrosis. These efforts have been intended to increase the cardiac function in such areas. Such cells delivered may be for example prepared from cultures of the patient's own cells, which may be cardiac cells for example, but may also be skeletal cells, fibroblasts or stem cells. The delivered cells may also be modified in a manner to enhance their contractile function or conductivity, and including to enhance their expression of certain factor(s), such as for example to enhance expression of connexin 43, a protein known to enhance cardiac signal conduction.
Connexins are found in connexons of gap junctions. Gap junctions regulate intercellular passage of molecules, including inorganic ions and second messengers, thus achieving electrical coupling of cells via gap junctions. Connexin proteins are the major gap junction protein involved in the electrical coupling of cells. For example Connexin 43 is the major gap junction protein in ventricular myocardium responsible for gap junction intercellular communication. Connexin 43, abbreviated herein as “Cx43”, is a protein having structural, regulatory, or biochemical functions associated with gap junctions and electromechanical coupling. Connexins are a whole family of proteins. There are specific connexins for various parts of the heart. Examples of Cx43 useful in the aspects of the invention providing for agent delivery into specified cardiac tissue regions associated with cardiac activation are polypeptide sequences such as human Cx43 (Genbank Accession Nos. XP—027460, XP—027459, XP—004121, P17302, AAD37802, A35853, NP—000156 and AAA52131), mouse Cx43 (Genbank Accession Nos. P23242, P18246, A39802, A36623, NP—034418, CM44640) and exemplary sequences for Rat Cx43 are found at Genbank Accession Nos. P08050, S00532, NP—036699, AAA75194 and 1404339A. Connexin family in the cardiovascular system includes Cx37, Cx40, Cx43, Cx45.
Various references herein to cardiac conduction, signal conduction, or otherwise “conduction” through cardiac tissue are generally intended to mean this propagation related to a resulting contractile wave through cellular tissue, including via gap junctions.
Other examples have been disclosed for locally delivering agents into cells resident in the target cardiac tissue structure that modify the cellular function in-vivo, such as by altering the genetic material within cells to enhance conduction/contraction, such as for example by enhancing cellular expression of certain compounds or agents that cause the intended effect (e.g. DNA material to cause expression or over expression of Cx43 or other such compounds).
There is yet to be a system or treatment method developed that combines cardiac stimulation systems, such as pacemakers or defibrillators, with delivery of conductive agents, such as cell therapy, gene therapy, other modes of tissue engineering, or other conductive agents such as conducting polymers, metals, or combinations thereof (such as injectable solutions or suspensions, e.g. gold, conducting “dust”, etc.), in a manner that substantially enhances the artificial stimulation such as pacing or defibrillating of cardiac tissue structures.
In recent years, biventricular septal pacing is an area that has received increasing attention and interest for new product development and research in recent years, in particular as it is intended as a curative measure for the complex and dangerous conditions of bundle block (e.g. bundle of His) and congestive heart failure.
Normal electrical activation of the ventricles generally proceeds as follows. Electrical impulse is initiated from the sinus node, leading to atrial activity passed through the AV node, followed by ventricular activation. The ventricular activation phase includes the following events (typically in the sequence described):                A) Activation of the left septum due to branches of the bundle of His entering the septum higher on the left side of the septum versus the right;        B) Apical depolarization follows early depolarization of the RV (depolarization of the RV occurs quickly due to the thinness of the RV);        C) Depolarization of the lateral wall of the left ventricle; and        D) Late LV depolarization of the base        
Various different disease states or abnormal conditions can affect this ventricular activation phase of the cardiac cycle. One such example of particular concern is called left bundle branch block (“LBBB”). LBBB alters the entire ventricular depolarization pathway. Depolarization starts from the right side of the septum and progresses toward the left front of the LV. Apical depolarization then occurs.
Biventricular pacing devices and methods have been disclosed that are generally intended to resynchronize LV contractility by activating the LV with a pacing lead, typically via a left-sided (e.g. left ventricle) pacing lead.
Further examples of systems, devices, and methods providing additional background related to the present invention are variously disclosed in the following U.S. Patent Application Publications: US 2002/0035388 to Lindemans et al.; and US 2002/0087089 to Ben-Haim. Other such examples are variously disclosed in the following U.S. Pat. No. 4,399,818 to Money; U.S. Pat. No. 5,103,821 to King; U.S. Pat. No. 5,683,447 to Bush et al.; U.S. Pat. No. 5,728,140 to Salo et al.; U.S. Pat. No. 6,059,726 to Lee et al.; U.S. Pat. No. 6,101,410 to Panescu et al.; U.S. Pat. No. 6,128,535 to Maarse; U.S. Pat. No. 6,151,525 to Soykan et al.; and U.S. Pat. No. 6,238,429 to Markowitz et al. Still other examples are disclosed in the following PCT Patent Application Publications: WO 90/10471 to King; WO 98/02150 to Stokes et al.; WO 98/28039 to Panescu et al.; WO 00/59375 to Sen; WO 01/68814 to Field; WO 02/22206 to Lee; and WO 2/051495 to Ideker et al. The disclosures of all these references listed in this paragraph are herein incorporated in their entirety by reference thereto.
There is still a need for improved cardiac stimulation systems and methods.
There is also still a need to improve conduction within cardiac tissue structures during cardiac stimulation.
There is in particular still a need for a biventricular septal stimulation system and method, such as for biventricular pacing, that provides for artificial cardiac stimulation in combination with delivery of conductive agents in order to enhance the stimulation effect.
There is also still a particular need for septal stimulation system and method that can capture a substantial region of septal tissue, such as in order to provide biventricular pacing in the setting of multiple left bundle branch block.